Juliann Chmielecki with Evolutionary Cancer Modeling Small Cell Lung Cancer − Optimization of Dosing for EGFR-Mutant Non

strategies. models based on the characteristics of diverse cancer cell types could offer clues for designing optimal treatment utility of evolutionary mathematical modeling in designing cancer treatments. If they prove beneficial, individual will have to come from patients. Clinical trials based on these alternative dosing strategies will be the true test of the resistance to prevent fast overgrowth by the sensitive cells, a result also born out in vitro and in vivo. Ultimate proof prediction. Modeling also indicated the wisdom of prolonging treatment with the EGFR TKI after the development of with high-dose pulses of an EGFR TKI should delay the onset of resistance. Subsequent cellular studies bore out this combined different treatment regimes. Their models predicted that continuous administration of a low-dose EGFR TKI under Understanding the growth dynamics of how tumors behave allowed the authors to calculate what would happen based on the differential growth rates of TKI-sensitive and TKI-resistant cells in heterogeneous tumor cell populations. therapy after a drug holiday. The authors then constructed an evolutionary mathematical model of tumor behavior disease progression, and patients with acquired resistance have re-responded to tyrosine kinase inhibitor (TKI) observations corroborated these findings. For example, patients with resistant tumors showed a slow course of their sensitive counterparts, and resistance was not maintained in the absence of selection. Multiple clinical which is activated in a subset of NSCLCs. To the authors' surprise, the drug-resistant cells grew more slowly than drugs used to treat NSCLC that are directed against the epidermal growth factor receptor (EGFR) tyrosine kinase, −− cancer cells. The authors made paired isogenic cell lines that were sensitive and resistant to afatinib and erlotinib mathematical model that predicted alternative therapeutic strategies to delay the development of drug-resistant growth characteristics of these cells were consistent with patient tumor behavior, enabling construction of a cancer (NSCLC) before and after the cells acquire resistance to targeted therapy, which inevitably they do. The small cell lung − how to better fight the potent forces of evolution, Chmielecki et al. examined the behavior of non on characteristically compliant cancer cells, as the common recurrence of drug-resistant cancers testifies. To learn molecular changes that strengthen the clan's chances of survival. Therapeutic drugs exert a powerful selective force Like any organism under severe evolutionary pressure, a few select members of a cancer cell population acquire